July 27, 2021
A very interesting lesson has been learned from observing combat related Traumatic Brain Injury (TBI). A review, coauthored by a researcher in Wuhan, describes how TBI includes both primary and secondary impairments. Iron overload and ferroptosis highly involved in the pathophysiological process of secondary brain injury. Ferroptosis is a form of regulatory cell death, as increased iron accumulation in the brain leads to lipid peroxidation, reactive oxygen species (ROS) production, mitochondrial dysfunction and neuroinflammatory responses, resulting in cellular and neuronal damage.
ACCELERATED AGING AFTER BRAIN INJURY
Traumatic brain injury (TBI) causes long-term structural and functional alterations to the brain. Some of
these changes are thought to be progressive in nature. It has also been determined that those with even mild head injuries are at an elevated risk for death for 15 years post injury.
The hallmark feature of ferroptosis is the iron-dependent accumulation of oxidatively damaged phospholipids (i.e., lipid peroxides). This is also a hallmark of SARS-CoV-2 (see image with (2)).
AN "EXPRESS TRAIN" TO A "NATURAL" DEATH
The end result of this cascade is as unique as each individual. Our deaths may be programmed within us. Ferroptosis is the bullet train to the mechanism of our deaths. Aging is associated with imbalances of iron metabolism.
In chess, there must be an imbalance for a player to die. Homeostasis, an "equal position," is the sign of a healthy position.
If the Spike Protein causes trauma, and brain trauma in particular, then this imbalance is created. If balance cannot be restored, death will follow.
We frame ourselves as our own murderer.
The perfect crime.
The Role of Iron, Its Metabolism and Ferroptosis in Traumatic Brain Injury
Metabolic Implications of Oxidative Stress and Inflammatory Process in SARS-CoV-2 Pathogenesis: Therapeutic Potential of Natural Antioxidants
Implication of ferroptosis in aging